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COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence
The liver is frequently affected by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection. The most common manifestations are mildly elevated alanine aminotransferase and aspartate aminotransferase, with a prevalence of 16-53% among patients. Cases with severe coronavirus disease 20...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
XIA & HE Publishing Inc.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8516829/ https://www.ncbi.nlm.nih.gov/pubmed/34722191 http://dx.doi.org/10.14218/JCTH.2020.00140 |
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author | Idalsoaga, Francisco Ayares, Gustavo Arab, Juan Pablo Díaz, Luis Antonio |
author_facet | Idalsoaga, Francisco Ayares, Gustavo Arab, Juan Pablo Díaz, Luis Antonio |
author_sort | Idalsoaga, Francisco |
collection | PubMed |
description | The liver is frequently affected by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection. The most common manifestations are mildly elevated alanine aminotransferase and aspartate aminotransferase, with a prevalence of 16-53% among patients. Cases with severe coronavirus disease 2019 (COVID-19) seem to have higher rates of acute liver dysfunction, and the presence of abnormal liver tests at admission signifies a higher risk of severe disease during hospitalization. Patients with chronic liver diseases also have a higher risk of severe disease and mortality (mainly seen in patients with metabolic-associated fatty liver disease). Several pathways of damage have been proposed in the liver involvement of COVID-19 patients; although, the end-cause is most likely multifactorial. Abnormal liver tests have been attributed to the expression of angiotensin-converting enzyme 2 receptors in SARS-CoV-2 infection. This enzyme is expressed widely in cholangiocytes and less in hepatocytes. Other factors attributed to liver damage include drug-induced liver injury, uncontrolled release of proinflammatory molecules (“cytokine storm”), pneumonia-associated hypoxia, and direct damage by the infection. Hepatic steatosis, vascular thrombosis, fibrosis, and inflammatory features (including Kupffer cell hyperplasia) are the most common liver histopathological findings in deceased COVID-19 patients, suggesting important indirect mechanisms of liver damage. In this translational medicine-based narrative review, we summarize the current data on the possible indirect mechanisms involved in liver damage due to COVID-19, the histopathological findings, and the impact of these mechanisms in patients with chronic liver disease. |
format | Online Article Text |
id | pubmed-8516829 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | XIA & HE Publishing Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-85168292021-10-28 COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence Idalsoaga, Francisco Ayares, Gustavo Arab, Juan Pablo Díaz, Luis Antonio J Clin Transl Hepatol Review Article The liver is frequently affected by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection. The most common manifestations are mildly elevated alanine aminotransferase and aspartate aminotransferase, with a prevalence of 16-53% among patients. Cases with severe coronavirus disease 2019 (COVID-19) seem to have higher rates of acute liver dysfunction, and the presence of abnormal liver tests at admission signifies a higher risk of severe disease during hospitalization. Patients with chronic liver diseases also have a higher risk of severe disease and mortality (mainly seen in patients with metabolic-associated fatty liver disease). Several pathways of damage have been proposed in the liver involvement of COVID-19 patients; although, the end-cause is most likely multifactorial. Abnormal liver tests have been attributed to the expression of angiotensin-converting enzyme 2 receptors in SARS-CoV-2 infection. This enzyme is expressed widely in cholangiocytes and less in hepatocytes. Other factors attributed to liver damage include drug-induced liver injury, uncontrolled release of proinflammatory molecules (“cytokine storm”), pneumonia-associated hypoxia, and direct damage by the infection. Hepatic steatosis, vascular thrombosis, fibrosis, and inflammatory features (including Kupffer cell hyperplasia) are the most common liver histopathological findings in deceased COVID-19 patients, suggesting important indirect mechanisms of liver damage. In this translational medicine-based narrative review, we summarize the current data on the possible indirect mechanisms involved in liver damage due to COVID-19, the histopathological findings, and the impact of these mechanisms in patients with chronic liver disease. XIA & HE Publishing Inc. 2021-10-28 2021-06-16 /pmc/articles/PMC8516829/ /pubmed/34722191 http://dx.doi.org/10.14218/JCTH.2020.00140 Text en © 2021 Authors. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0), permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Idalsoaga, Francisco Ayares, Gustavo Arab, Juan Pablo Díaz, Luis Antonio COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence |
title | COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence |
title_full | COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence |
title_fullStr | COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence |
title_full_unstemmed | COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence |
title_short | COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence |
title_sort | covid-19 and indirect liver injury: a narrative synthesis of the evidence |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8516829/ https://www.ncbi.nlm.nih.gov/pubmed/34722191 http://dx.doi.org/10.14218/JCTH.2020.00140 |
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